氧化应激在中暑大鼠急性肝损伤中的作用及机制研究

发布时间：2018-10-04 19:24

【摘要】：目的探讨氧化应激在中暑急性肝损伤发生中的作用及其可能机制。方法 32只大鼠按随机数字表法分为4组:假加热正常对照组(Sham组)、中暑组(HS组)、假加热N-乙酰半胱氨酸治疗组(Sham-NAC组)以及中暑NAC治疗组(HS-NAC组),每组8只。通过人工气候舱制备中暑大鼠模型,监测大鼠直肠温度(Tr)、脉率(HR)、收缩压(SBP)。记录中暑发生的时间。于中暑开始后12h处死大鼠,测定大鼠血清丙氨酸氨基转移酶(ALT)和总胆红素(TBIL)水平,以及肝脏组织匀浆IL-6、IL-1β、TNF-α、丙二醛(MDA)、总超氧化物歧化酶(T-SOD)和谷胱甘肽(GSH)等指标的变化,组织学观察肝脏氧自由基(ROS)含量、中性粒细胞浸润以及病理损伤情况。结果中暑发生时HS-NAC组与HS组Tr、HR、SBP、中暑发生时间等比较差异无统计学意义(P0.05),但HS-NAC组的生存时间与HS组相比明显延长,差异有统计学意义(P=0.039)。中暑发生后12h,HS组肝组织匀浆中ROS和MDA含量及血清ALT和TBIL水平较其他3组明显升高(P=0.000),肝组织匀浆中T-SOD和GSH含量较其他3组明显下降(P=0.000)。病理观察显示HS-NAC组肝损伤较HS组减轻(P=0.000)。HS组肝脏中性粒细胞浸润水平及IL-6、IL-1β、TNF-α浓度均明显高于HS-NAC组(P=0.000)。结论氧化应激在中暑肝损伤中起重要作用,其机制可能与直接细胞毒和介导炎症反应有关。
[Abstract]:Objective to investigate the role of oxidative stress in the development of acute hepatic injury due to heat stroke and its possible mechanism. Methods Thirty-two rats were randomly divided into four groups: sham heating normal control group (Sham group), heatstroke group (HS group), pseudothermic N-acetylcysteine treatment group (Sham-NAC group) and heatstroke NAC treatment group (HS-NAC group) with 8 rats in each group. The rat model of heatstroke was established by artificial climate chamber, and the (Tr), pulse rate of rectal temperature was monitored by (HR), systolic pressure (SBP). Record the time of heat stroke. The rats were killed 12 hours after heatstroke. The levels of serum alanine aminotransferase (ALT) and total bilirubin (TBIL), and the changes of liver homogenate IL-6,IL-1 尾 TNF- 伪, malondialdehyde (MDA), total superoxide dismutase (T-SOD) and glutathione (GSH) were measured. Liver oxygen free radical (ROS) content, neutrophil infiltration and pathological injury were observed histologically. Results there was no significant difference in the duration of Tr,HR,SBP, heatstroke between HS-NAC group and HS group (P0.05), but the survival time of HS-NAC group was significantly longer than that of HS group (P0. 039). The contents of ROS and MDA in liver tissue homogenate and serum ALT and TBIL levels in HS group were significantly higher than those in other three groups (P0. 000). The contents of T-SOD and GSH in liver tissue homogenate were significantly lower than those in other 3 groups (P0. 000). Pathological observation showed that the liver injury in HS-NAC group was less than that in HS group (P0. 000). The level of neutrophil infiltration and the concentration of IL-6,IL-1 尾-TNF- 伪 in HS group were significantly higher than those in HS-NAC group (P0. 000). Conclusion oxidative stress plays an important role in heatstroke liver injury and its mechanism may be related to direct cytotoxicity and inflammatory response.
【作者单位】：解放军303医院重症医学科;广州军区广州总医院重症医学科;南方医科大学抗体工程研究所;
【基金】：国家自然科学基金(81671896,81471839) 中国博士后科学基金(2012M512181) 广西省自然科学基金(2016GXNSFAA380313) 广东省自然科学基金(2016A030310288,2014A030313601) 广东省科技计划项目(2013B031800010)~~
【分类号】：R594.12

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